Introduction: There are currently no reports in the literature regarding changes in end-tidal carbon dioxide (ETCO(2)) when the small bowel is deliberately or inadvertently perforated during laparoscopic surgery. The aim of this study was to assess the influence of small bowel perforation during laparoscopy on ETCO(2) in a rat model.
Materials And Methods: Two groups of Wistar rats (n = 8/group) were anesthetized, tracheostomized, and mechanically ventilated at a fixed tidal volume and respiratory rate. After a stabilization phase of 30 min, CO(2) pneumoperitoneum was established to 5 mmHg in one group and 12 mmHg in the other group, and maintained for 30 min. A small bowel perforation was then created and pneumoperitoneum was reestablished for another 30 min. Blood pressure, heart rate, peak ventilatory pressure, and ETCO(2) were recorded throughout the experiment.
Results: No significant changes in blood pressure throughout the experiment were noted in either group. The ventilatory pressure increased in both groups after the induction of pneumoperitoneum. In the 5 mmHg group, there was a modest increase in ETCO(2) following the induction of pneumoperitoneum (from 39.4 +/- 1.9 to 41.1 +/- 1.4, P = 0.014), and a further increase following the small bowel perforation (from 41.1 +/- 1.4 to 42 +/- 0.8, P = 0.007). In the 12 mmHg group, there was no change in ETCO(2) after the induction of pneumoperitoneum; however, there was a substantial increase in ETCO(2) following bowel perforation (35.0 +/- 2.0 to 49.8 +/- 7.1, P = 0.002).
Conclusions: ETCO(2) increases when the small bowel is perforated during CO(2) pneumoperitoneum. This increase seems more substantial under higher pneumoperitoneal pressures. Small bowel injury may enable the diffusion of CO(2) through the bowel mucosa, causing ETCO(2) elevation. Therefore, an abrupt increase in ETCO(2) observed during laparoscopy may indicate small bowel injury.
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